Aim. To identify the risk factors of kidney injuries in hypertensive patients with uric acid (UA) metabolic disorders in order to choose the optimal management tactics, by analyzing the changes in markers for endothelial dysfunction (endothelin-1 (ET-1), microalbuminuria (MAU), intima-media thickness (IMT)) and tubulointerstitial tissue lesion (2-microglobulin (2-MG, monocyte chemotactic protein-1 (MCP-1)). Subjects and methods. Eighty-one patients with grade 1 hypertension without associated diseases, diabetes mellitus, or metabolic syndrome were examined. There were 3 study groups: 1) hyperuricosuria (n=7); 2) hyperuricemia (n=53); 3) hyperuricemia and renal failure (n=6); and a control group of 15 hypertensive patients without UA metabolic disorders who were matched for age and gender with the patients of the study groups. Results. The hypertensive patients with hyperuricemia, as compared with those without UA metabolic disorders, showed higher plasma concentrations of ET-1 (p=0.003) and MAU (p=0.009) and more marked increases in common carotid IMT (p=0.044), urinary excretion of 2-MG (p=0.010), and MCP-1 (p=0.030). There were direct correlations between all the examined biomarkers and the degree of uricemia (Rs=0.453; р<0.001; Rs=0.411; р<0.001; Rs=0.322; р=0.067; Rs=0.537; р<0.001; and Rs=0.318; р=0.004, respectively) and between the markers of endothelial dysfunction and those of tubulointerstitial tissue lesion (Rs=0.295 for ET-1 and MCP-1; р=0.008; Rs=0.399 for ET-1 and 2-MG; р<0.001; Rs=0.462 for MAU and 2-MG; р<0.001; and Rs=0.188 for MAU and MCP-1; р=0.094). Multivariate analysis of the clinical and laboratory parameters under study confirmed the role of serum MCP-1, 2-MG, MAU, creatinine levels as independent predictors for decreased relative urinary gravity, the clinical sign of tubulointerstitial tissue lesion/fibrosis, and that of a wider range of the indicators, such as MAU, ventricular septal thickness, glomerular filtration rate, relative urinary gravity, systolic blood pressure, MPC-1, low-density lipoproteins, as risk factors for renal filtrating dysfunction.